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PubMed1982

How does interferon inhibit tumour growth?

Interferon can inhibit tumour growth in experimental animals and in some patients with benign and malignant tumours. There is experimental evidence to suggest that several mechanisms may be involved: a direct effect on the tumor or an indirect effect via the host, or both. Thus, interferon may slow the rate of tumour cell multiplication and this may lead to cell death. Interferon may induce changes in the cell surface rendering tumour cells more sensitive to host defence mechanisms. Interferon may induce reversion in the phenotype of tumour cells. Interferon may stimulate specific and non-specific humoral and cellular host mechanisms. The relative importance of these different effects of interferon may vary depending on the host and the particular tumour.

Animals↗
PubMed1976

Effects of the phage P1 restriction system on coliphage phi W: degradation and complex formation of phage phi W DNA.

Growth of phages phi W and T7 was restricted in Escherichia coli lysogenic for phage P1. Only a fraction of the infected cells gave burst of phages. Cells permitting phage growth gave normal burst size. Host strains carrying P1 mutants with defective endonuclease gave no restriction of phages T7 and phi 3, the latter a host-range mutant of phi W. Degradation but not modification of parental phage DNA could be demonstrated. Although no DNA, RNA or protein was synthesized in phi W infected P1 lysogenic cells, the parental phage DNA was found in increasingly larger complexes during the course of infection. At early times after infection, parental phage DNA was found to sediment about twice as fast as mature phage DNA. At later times during the infection the parental phage DNA was recovered as a very rapidly sedimenting material. Such material was also found in alkaline sucrose gradient centrifugation after treatment of the cell extract with sodium dodecyl sulphate, pronase digestion and phenol extractions.

Coliphages↗
PubMed1976

The RNAs of the defective interfering Pichinide virus.

A Pichinde persitently infected BHK21/13S culture was established in which defective interfering (DI) virus continued to be synthesized after cessation of plaque-forming virus replication. This DI virus, concentrated from NaCl-polyethylene glycol treated tissue culture fluids, was shown to band over a much broader range than standard virus, in either discontinuous or continuous sucrose gradients. The polyacrylamide gel profile of the RNAs extracted from standard virus contained six components with sedimentation coefficients corresponding to 31, 28, 22, 18, 15 and 4-6S. All RNAs extracted from DI virus preparations, however, did not contain the 22 and 15S species. Furthermore, a new 20S fraction was observed in DI virus taken from cultures which had been maintained for more than 175 generations after the initial infection, whereas it was absent in DI virus synthesized prior to that time.

Arboviruses↗